作者: Zaiting Ye , Bingmu Fang , Jiongwei Pan , Ning Zhang , Jinwei Huang
DOI: 10.3892/OR.2017.5619
关键词:
摘要: The present study determined the role and mechanism of miR-138 in non-small cell lung cancer (NSCLC). In total, 45 freshly resected clinical NSCLC tissues were collected. expression lines by real-time quantitative PCR. mimics transfected into A549 Calu-3 cells vitro, then effects on proliferation, cycle, invasion metastasis investigated CCK-8 assay, Transwell flow cytometry, respectively. protein potential target gene Sirt1 western blot analysis. Dual-luciferase reporter assay was performed to further confirm whether miR-138. significantly lower negatively correlated differentiation degree lymph node cancer. vitro experiment results showed that inhibited migration. It verified could downregulate expression, inhibit epithelial-mesenchymal transition (EMT), decrease activity AMPK signaling pathway elevate mTOR phosphorylation level. demonstrated directly regulate Sirt1. Downregulation alone can also cause same molecular biological function changes. Western analysis confocal microscopy indicated overexpression or interference autophagy possibly through AMPK-mTOR pathway. plays a tumor suppressor may migration downregulation activation autophagy. is closely related development